TY  - JOUR
A1  - Chillo, Omary
A1  - Kleinert, Eike Christian
A1  - Lautz, Thomas
A1  - Lasch, Manuel
A1  - Pagel, Judith-Irina
A1  - Heun, Yvonn
A1  - Troidl, Kerstin
A1  - Fischer, Silvia
A1  - Caballero-Martinez, Amelia
A1  - Mauer, Annika
A1  - Kurz, Angela R. M.
A1  - Assmann, Gerald
A1  - Rehberg, Markus
A1  - Kanse, Sandip M.
A1  - Nieswandt, Bernhard
A1  - Walzog, Barbara
A1  - Reichel, Christoph A.
A1  - Mannell, Hanna
A1  - Preissner, Klaus T.
A1  - Deindl, Elisabeth
T1  - Perivascular Mast Cells Govern Shear Stress-Induced Arteriogenesis by Orchestrating Leukocyte Function
JF  - Cell Reports
N2  - The body has the capacity to compensate for an occluded artery by creating a natural bypass upon increased fluid shear stress. How this mechanical force is translated into collateral artery growth (arteriogenesis) is unresolved. We show that extravasation of neutrophils mediated by the platelet receptor GPIbα and uPA results in Nox2-derived reactive oxygen radicals, which activate perivascular mast cells. These c-kit+/CXCR-4+ cells stimulate arteriogenesis by recruiting additional neutrophils as well as growth-promoting monocytes and T cells. Additionally, mast cells may directly contribute to vascular remodeling and vascular cell proliferation through increased MMP activity and by supplying growth-promoting factors. Boosting mast cell recruitment and activation effectively promotes arteriogenesis, thereby protecting tissue from severe ischemic damage. We thus find that perivascular mast cells are central regulators of shear stress-induced arteriogenesis by orchestrating leukocyte function and growth factor/cytokine release, thus providing a therapeutic target for treatment of vascular occlusive diseases.
KW  - Mast cells
Y1  - 2016
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-164800
VL  - 16
IS  - 8
ER  -